RESUMO
Neuroscientific research has consistently shown more extensive non-visual activity in the visual cortex of congenitally blind humans compared to sighted controls; a phenomenon known as crossmodal plasticity. Whether or not crossmodal activation of the visual cortex retracts if sight can be restored is still unknown. The present study, involving a rare group of sight-recovery individuals who were born pattern vision blind, employed visual event-related potentials to investigate persisting crossmodal modulation of the initial visual cortical processing stages. Here we report that the earliest, stimulus-driven retinotopic visual cortical activity (<100 ms) was suppressed in a spatially specific manner in sight-recovery individuals when concomitant sounds accompanied visual stimulation. In contrast, sounds did not modulate the earliest visual cortical response in two groups of typically sighted controls, nor in a third control group of sight-recovery individuals who had suffered a transient phase of later (rather than congenital) visual impairment. These results provide strong evidence for persisting crossmodal activity in the visual cortex after sight recovery following a period of congenital visual deprivation. Based on the time course of this modulation, we speculate on a role of exuberant crossmodal thalamic input which may arise during a sensitive phase of brain development.
Assuntos
Cegueira , Córtex Visual , Humanos , Percepção Visual , Som , TálamoRESUMO
Increasing rates of preterm births coupled with better survival of these infants have resulted in higher prevalence of systemic and ocular complications associated with prematurity. In addition to retinopathy of prematurity, infants who are born preterm may suffer from severe visual impairment as a result of hypoxic ischemic encephalopathy, hypoglycemia, and other metabolic imbalances. The effect of these processes on the anterior visual pathway may result in optic atrophy, optic nerve hypoplasia or optic disc cupping and affection of the posterior visual pathway leads to cortical visual impairment (CVI). Other ocular associations include strabismus, nystagmus, and ocular motor abnormalities such as tonic down gaze and defective saccades and pursuits. Cortical and subcortical involvement also manifests as defects in functional vision and these have not yet been completely understood. Children with CVI may have visual field defects, photophobia, defective visual processing, and deficient color vision. Since most of these children also suffer from additional systemic disabilities, evaluation, and management remains a challenge. However, early diagnosis and initiation of rehabilitation therapy can prove to be of significant benefit in these children.